Eye (1988) 2, Suppl S27-S36

Childhood Blindness

ALLEN FOSTER*

London

The presentation of a blind child is a relatively Thble I Classification of Aetiological Factors in uncommon occurrence for most ophthalmolo­ Childhood Blindness gists, however worldwide there are over one Factors operating from conception (Genetically million blind children and many more with determined) severe . This review considers e.g. familial the patterns of childhood blindness in different congenital retinal aplasia parts of the world with particular emphasis on retinoblastoma recent findings from Africa. tapeto-retinal degeneration In discussing childhood blindness certain albinism difficulties must be recognised. First, there is a malformations paucity of data on prevalence and causes of childhood blindness. Secondly, the available data Factors operating during the intra-uterine period use different definitions of blindness and e.g. rubella classifications of the causes of blindness. toxoplasmosis Thirdly, the method of obtaining the data varies, syphilis including blind registrations, community based toxins/drugs surveys and examination of children in blind schools. All these factors make comparisons Factors operating at birth or in the immediate between the available data unsatisfactory. This perinatal period e.g. of prematurity acknowledged, there is value in attempting to hypoxia resulting in damage to the visual look at the differences in prevalence and causes pathways of blindness in different areas of the world, in ophthalmia neonatorum order to identify priorities for the prevention of unnecessary blindness in children. Factors operating in childhood e.g. Geographical Variations measles The causes of childhood blindness can be external eye infections usefully considered according to the trauma classification given in Table I. In Europe and meningo/encephalitis North America, genetic factors are responsible for between 30-50% of cases, with familial scarring from and ocular infections and hereditary retinal are responsible for up to 25% of childhood diseases being largely responsible. Other blindness in Latin America, occurring more important causes result from problems at frequently in rural areas. The importance of childbirth and in the perinatal period causing malnutrition in South America may not be retinopathy of prematurity, and optic atrophy reflected in the statistics from blind school due to hypoxia from brain damage. (Table II.) In surveys, where the children tend to come from the Caribbean and partsof South America, intra­ the cities in which hereditary factors and intra­ uterine infections, particularly rubella, are a uterine infections predominate. (Table III.) In major cause of childhood blindness (4). Corneal the Mediterranean and Middle East, hereditary

*Senior Lecturer in Preventive Ophthalmology, Medical Consultant to Christoffel Blindenmission. Correspondence to: Allen Foster, FRCS, DO, Department of Preventive Ophthalmology, Institute of Ophthalmology, 27 Cayton Street, London ECIV 9El. 528 ALLEN FOSTER

Table II Anatomical cause of Childhood Blindness in England calculated from blind registrations Europe and North America by % between 1969-1976 is 0.09/1000 (0-4 years) and 0.23/1000 (5-15 years) giving a total of Country USA (1) Edinburgh (2) Norway (3) approximately 2,300 children registered blind.ll No. of Blind Children 16 states n = 99 n = 534 lear 1970 1987 1985 In comparison a survey in Bangladesh gave a prevalence of binocular blindness of 0.64/1 000

Corneal Scar / for children aged 0-5 years from rural areas, and Phthisis 2 0 1.09/1000 for children from urban slums.12 The Cataract 13 12 10 best available data in Africa is from a survey of 3 1 0 5,436 children aged 0-5 years in the Lower Shire Retinal disease 33 36 42 Valley of Malawi, where the prevalence of Optic atrophy 9 16 14 bilateral blindness was 1.11100013 - 12 times 0 2 0 greater than for England. (Table IV.) However, Whole eye/others/ Unknown 40 31 34 these figuresare likely to underestimate the size e.g. malformations of the problem, because at least 50% of children cortical blindness who become blind in developing countries die albinism within the next 12 months from infections, malnutrition and neglect. 12 Table III Anatomical cause of Childhood Blindness in A conservative estimate for Africa would Jamaica. Peru and Bolivia by % suggest that there are 150,000blind children aged

Country Jamaica (4) Peru (5) Bolivia (6) CAUSES OF CHILDHOOD BLINDNESS No. of Blind Children n = 108 n = 278 n = 78 Year 1986 1986 1988

EUROPE I N. AMERICA Corneal Scar/ Phthisis 5 9 23 Cataract 39 21 21 Uveitis 5 2 2 Retinal disease 15 28 23 Optic atrophy 18 10 10 Glaucoma 15 23 10 Whole eye/others/ unknown 3 7 11

Rubella infection 22 ? 12 CARIBBEAN LATIN AMERICA factors, in part due to consangUinIty are reported to account for 77% (Lebanon), 79% (Cyprus), and 84% (Saudi Arabia) of childhood blindness.7,8,9 This contrasts with large parts of Africa and Asia where nutritional factors, and ocular infections account for more than half of all childhood blindness. 10 In Asia, diarrhoea is the important predisposing factor for vitamin A deficiency and blindness from corneal scarring, AFRICA whilst in Africa up to 50% of childhood blindness is associated with recent measles infection. Figure 1 summarises the geographical variations in the causes of blindness in children.

Prevalence of Childhood Blindness The prevalence of childhood blindness III Figure 1 CHILDHOOD BLINDNESS 829

Table IV Geographical variations in the prevalence and major factors causing Childhood Blindness

Estimated No. of Blind Children Prevalence/WOO children Major factors (0-15 years)

Europe and 0.09 (0-4 years) Hereditary. England - 2,300 North America Problems at birth:­ 0.23 (5-15 years) (particularly pre-term babies) USA - 12,000 (England)

Latin America ? Intra-uterine infections. 60,000 - 90,000 and Caribbean (Nutritional/Measles in rural areas)

Asia 0.64 (0-5 years) Nutritional/Diarrhoea 400,000 - 900,000 (Bangladesh - rural)

1.09 (0-5 years) (Bangladesh - urban)

Africa 1.1 (0-5 years) Nutritional/Measles. 250,000 - 400,000 (Malawi) Lack of eye services.

Table V Anatomical cause of Blindness in African Children by %

EASI AFRICA WEST AFRICA - SAHEL WEST AFRICA - COASIAL Country Kenya Ethiopia Tanzania Malawi Tanzania Nigeria Mali Ghana Togo Nigeria (14) (15) (16) (17) (IS) (north) (north-west) (south) (south-west) No. of Blind (19) (20) (21) (22) (23) Children 749 195 426 270 72 104 73 65 54 140

Corneal Scar/ Phthisis 49 72 71 75 67 69 45 63 43 22 Cataract 10 6 7 3 18 3 5 5 9 19 Uveitis 5 4 5 ° ° 5 14 6 6 5 Retinal disease 2 3 4 4 11 6 10 9 11 Optic atrophy 11 1O 4 3 3 5 6 5 6 14 Glaucoma ° ° ° 4 9 8 16 14 Whole eye/others /unknown 23 5 8 18 7 3 15 3 11 15

% Ass. with 31 27 37 44 ? 29 ? 52 25 14 Measles infection

0-5 years and a similar figure aged 6-15 years, (a) Regional Iilriations giving a total of at least 300,000 blind children, Bilateral corneal scarring or is with 50,000 - 80,000 new cases per year, many responsible for 49-75 % of childhood blindness in of whom die. Bangladesh with a total population East Africa, 45-69% in the Sahel area of West of 94 million is estimated to have 30,000 children Africa and 22-43% on the coastal area of blinded each year of which 15,000 survive totally West Africa, but only 1-2 % of childhood blind, and a further 45,000 survive with blindness in Europe, 5% in Jamaica and 9-23% appreciable visual impairment from corneal in Latin America. Measles infection is asso­ damage or opacity. 12 ciated with 27-44% of childhood blindness in East Africa, 29-52% in the Sahel and 14-25 % Childhood Blindness in Africa in the coastal areas of West Africa. The dietary Table V summarises the data on the anatomical use of red palm oil, rich in vitamin A, in the cause of childhood blindness from 49 blind coastal (rain forest) areas of West Africa results schools and 2 hospitals in sub-Saharan African in less corneal blindness from countries. and associated measles infection compared S30 ALLEN FOSTER

AETIOLOGY Of CORNEAL ULCERATION with East Africa and the Sahel area of West Figure 2 IN AFRICAN CHILDREN

Africa. MALARIA LACK OF The other important causes of blindness in HE SERVICES African children are congenital cataract (3-19% ), uveitis (0-14% ), retinal disease (1-11% ), optic atrophy (3-14% ) and glaucoma (0-16% ). It is interesting to note that congenital/juvenile EPIDEMIC glaucoma only accounted for 1% of blindness in HAEMORRHAGIC MALNUTRITION East Africa, but 4-16% in West Africa. This would appear to be a true regional difference, but the reasons for it are not clear. There has been considerable discussion on the relative importance of vitamin A deficiency,14,24,25,26,27,28,29 measles30 and herpes simplex virusl9,31 in causing corneal ulceration, scarring and resultant blindness in different parts MALNUTRITION of Africa. The importance of these conditions varies from place to place, and from time to time depending on famine, measles epidemics and the availability of eye services. The inter-relation­ ship of different factors is important in planning any programme to reduce the amount of avoidable childhood blindness in Africa. DIAr.RHOEA DEHYDRATION (�al absorpt ion)

(b) Measles associated corneal ulceration simplex was responsible for 20% of Measles infection is usually accompanied by measles associated corneal ulcers in the , lacrimation and a superficial Tanzanian study. 32 Third, measles punctate kerato-conjunctivitis which lasts 2-10 conjunctivitis, causing red eyes together with the days. In Africa 1-4% of hospitalised children local knowledge that measles can result in with measles develop true corneal ulceration as blindness leads mothers to use Traditional Eye distinct from punctate keratitis, and the Medicines (TEM) in an effort to help their ulceration is bilateral in at least 50% of cases children. Many of these TEM are harmless, but (32). In a study from Tanzania measles infection occasionally they may lead to corneal ulceration was associated with 69% of corneal ulcers which and blindness. Lastly, measles produces subsequently resulted in bilateral blindness.32 anorexia and gastroenteritis resulting in a This confirms the finding from blind school decrease in supply of vitamin A and protein to a surveys given in Table V where measles is child who may already have marginal liver associated with one quarter to one half of all reserves of vitamin A. At the same time the childhood blindness and 50-80% of corneal increase in demand for vitamin A associated blindness in children. with measles infection results in a sudden The pathways by which measles leads to decompensation in vitamin A metabolism. The corneal ulceration are complex. First the ocular manifestation of this deficiency is measles virus may cause a superficial confluent necrosis of the corneal stroma, often in both eyes keratitis, particularly in the exposed area of the and in severe cases from limbus to limbus , which can lead to a central epithelial (keratomalacia). This bilateral, deep and ulcer. This occurs especially in dehydrated perforating corneal ulceration is responsible for children, lying with exposed . Second, most of the blindness in African children. measles causes fever and a depression of cell­ Figure 2 summarises the pathways by which mediated immunity. Both these factors may measles may lead to corneal ulceration. predispose to herpes simplex infection. Herpetic Ulceration due to herpes simplex virus or stomatitis is common following measles measles keratitis/exposure is usually unilateral infection in African children19,3 1 and herpes and superficial, and therefore rarely causes CHILDHOOD BLINDNESS S31

Fig. 3. Amoeboid herpetic ulcer in a young Tanzanian child with measles. childhood blindness. However, TEM and vita­ corneal scarring with visual loss. Fortunately min A deficiency cause bilateral and deep ulcers this is usually unilateral. Once the diagnosis is which are responsible for the majority of corneal made, treatment with topical antivirals is usually blindness. effective in healing the ulcer. In many areas of rural Africa antivirals are not readily available, (c) but it is possible to make idoxuridine drops Corneal ulceration due to herpes simplex virus relatively simply from the gallenical powder. has been well documented in Africa.19•32 The ulceration is more commonly geographic/ (d) Traditional Eye Medicines amoeboid than dendritic, bilateral in a quarter of Traditional eye medicines come in many forms cases and often occurring before the age of 2 including herbal medicines, lime juice, urine, years. (Figure 3.) These features are atypical of toothpaste, kerosene and breast milk to mention herpetic keratitis in Western countries. Besides but a few. Many are harmless and some may be measles other predisposing factors for herpetic beneficial, however corneal ulceration may be keratitis in African children are malnutrition caused by the caustic, physical or thermal trauma (particularly marasmus) and malaria. Clusters of of the TEM, or by secondary infection with patients with herpetic ulcers have been noted to fungi (from plant materials) or bacteria, occur towards the end of the rainy season when particularly Neisseria gonococcus (from urine). malaria is at its worst, and also occasionally in Measles is the major predisposing factor for association with epidemics of meningococcal corneal ulceration due to TEM in children. meningitis. Other factors which lead to clusters of these In areas where ophthalmic services are sparse, ulcers in children or adults are epidemics of viral the diagnosis of herpetic ulcer is often missed haemorrhagic conjunctivitis, lack of eye services and many of these children develop chronic and the particular practices of individual ulcers which result in quite severe superficial traditional healers. 832 ALLEN FOSTER

Fig. 4. Three areas of descematocoele in a Tanzanian girl after the application of Traditional Eye Medicines.

Fig. 5. Stromal necrosis with descematocoele formation in a Tanzanian child with measles associated cornelll ulceration due to vitamin A deficiency. CHILDHOOD BLINDNESS S33

The diagnosis of corneal ulceration due to neonatorum are the other causes of childhood TEM is based upon a positive history (which ulceration in Africa. Ophthalmia neonatorum may be very difficult to illicit), together with the due to Neisseria Gonococcus is relatively presence of chemical conjunctivitis and atypical common in some parts and is estimated to corneal ulcers (Figure 4). account for 2-5 % of childhood blindness. 32 Treatment of the ulcers is often unrewarding Penicillinase producing Neisseria is becoming unless there is a secondary infection which can an increasing problem in many African urban be treated with antibiotics or antifungals. Health situations. promotion, to inform the public through radio or In summary, childhood blindness in Africa, is press, about the danger of TEM particularly mainly due to corneal ulceration from vitamin A during epidemics of conjunctivitis can help, but deficiency, traditional eye medicines and herpes alternative eye care must be provided at the same simplex keratitis, all of which are associated time. Most traditional healers if correctly with measles infection. The other significant approached are very willing to use antibiotic eye cause of bilateral corneal ulceration is ointments instead of TEM, if the ointment is ophthalmia neonatorum. made freely available to them. The relative importance of each cause of corneal ulceration in different parts of Africa (e) Vitamin A Deficiency will depend on: The early signs of vitamin A deficiency are night (l) the prevalence of vitamin A deficiency and blindness (XN) and Bitot spots (XlB).33 These undernutrition in the childhood usually occur after the age of three years and are population. associated with a chronic dietary deficiency of (2) local practices in relation to measles vitamin A as is seen in Indonesia, Bangladesh infection - for example, the use of TEM, and recently Ethiopia.33,12,34 or the withholding of food and water. The corneal signs of vitamin A deficiency, (3) the prevalence of herpes simplex virus xerosis (X2) and (X3), occur in infection in children and their mothers. children with Malnutrition, Malabsorption These factors will vary in time and place (chronic diarrhoea) or Measles, and are most according to the availability of food, eye commonly seen between the ages of one and four services, and seasonal variations in infectious years. The ulcers are sometimes epithelial and diseases. may be due to an area of dry keratinised corneal epithelium being denuded. More commonly Prevention and Treatment however the morphology is a well-demarcated (a) Measles immunisation round or oval area of full thickness stromal 25%- 50% of all childhood blindness in Africa is necrosis often with intact epithelium (Figure 5). associated with measles. Immunisation at the The response to therapy if diagnosed early is age of nine months as recommended by most dramatic, with healing of the ulcer in 4-5 days, African countries would do much to reduce child leaving a residual corneal scar. mortality and childhood blindness. Herd The mortality in children with frank immunity can be expected when immunisation keratomalacia is high, exceeding 30% even with cover reaches 80% , but this figure is rarely treatment.32 Recent work from Indonesia and attained in many African countries, partly due to Tanzania now suggests that vitamin A deficiency, lack of public awareness, cost and the logistics of even sub-clinical, is responsible for an increased the immunisation programme, particularly risk of respiratory and diarrhoea infections in maintaining the cold chain. The Expanded children.35 Vitamin A administration to children Programme of Immunisation (EPI of World with measles in developing countries is now Health Organisation) is now extending the recommended by WHO and UNICEF, in order coverage of immunisation and it is to be hoped to reduce child mortality and childhood that there will be a consequent reduction in blindness.36,37 mortality and morbidity from blindness.

(f) Other causes of corneal ulceration (b) Improve vitamin A status in pre-school Trauma, bacterial infection, exposure from children proptosis and particularly ophthalmia There are three possible ways of improving the S34 ALLEN FOSTER vitamin A dietary intake of young children: schedules are suggested for areas of Africa (1) Education programme to make mothers where corneal ulceration and corneal scarring in and girls more aware of the importance of children occur, or where protein-energy readily available foods rich in vitamin A, malnutrition is a problem. e.g. dark green leafy vegetables, mangoes, Prophylactic administration of vitamin A, papaya and red palm oil. 200,000 IU orally, as a single dose should be (2) Distribution of vitamin A capsules given to children with: (200,000 I.v.), once every 4-6 months to - marasmus or kwashiorkor; either, all pre-school children or to only - chronic diarrhoea; those at high risk of developing - severe measles; xerophthalmia e.g. children with - night blindness, or Bitot's spots. malnutrition, chronic diarrhoea, measles If a child is seen with a suspected corneal ulcer, or early signs of vitamin A deficiency. then the following treatment is recommended: This has been tried in some countries with (1) Immediate administration of vitamin A, a limited amount of success. 12 200,000 IU orally (or injection of aqueous (3) Fortify with vitamin A a centrally vitamin A, 100,000 IU, if the child is processed food which is generally vomiting); repeat after one day and again available and consumed by pre-school after one week. (Half the dose for children children. Sugar would be most suitable, under one year of age.) however the cost of such a programme is (2) Antibiotic eye ointment (e.g. 1% considerable in terms of the resources tetracycline) three times per day. spent on health in many African countries. (3) Atropine eye ointment 0.5 %, once daily. All these programmes require political (4) An eye pad. determination, good administration and (5) General treatment for malnutrition, adequate infrastructure to achieve success. The diarrhoea and other systemic infections. nutrition education programme would have a If the corneal ulcer fails to improve within five long-lasting effect and is the most cost-effective days on this regimen, it may indicate infection approach, but probably needs to be implemented with herpes virus. This will require additional together with a short-term strategy e.g. treatment with anti-virals, or possibly distribution of vitamin A capsules to children at mechanical debridement of the corneal high risk. epithelium, if the ulcer is still superficial. It is very important for all health workers in (c) Ready availability of antibiotic eye ointment Africa to be on the lookout for the early The majority of African people live in rural development of corneal ulceration in any child areas where eye services are inadequate and eye with malnutrition or measles; failure by the child infections (epidemic conjunctivitis, , to open its eyes may be indicative of corneal ophthalmia neonatorum, and measles) are ulceration. common. Traditional Eye Medicines (herbal medicines) or Inappropriate Eye Therapies (e) Management of (kerosene, sugar water, antibiotic powders or Cataract in children, due either to hereditary steroid drops) are commonly used topically to factors, rubella or other causes accounts for treat these eye infections either by traditional 10-13% of blind registrations in industrialised healers or by self-administration. The ready countries (Table II), 21-39% in Latin America availability to rural people of an inexpensive, but and the Caribbean (Table III), and 3-19% in effective topical antibiotic (e.g. enriched Africa (Table V). tetracycline ointment 1% ) could do much to In Africa it is not uncommon to find school­ reduce blindness from corneal ulcers in children age children and even adolescents in blind and adults. schools with bilateral mature untreated , or the complications of unsuccessful surgery. In (d) Management of corneal ulceration in African one school eight of 14 aphakic eyes had blinding children surgical complications. IS The following prevention and treatment The early recognition, surgical treatment and CHILDHOOD BLINDNESS 835 management of in children is one 4 Moriarty B. Childhood Blindness in Jamaica. Br J priority in the reduction of childhood blindness. Ophthalmol 1988, 72: 65-7. This requires training of all medical workers in 5 Wong L. Personal communication. St. Francisco the recognition of cataract and the development Blind School. Lima. of tertiary eye centres in which there are 6 Personal Observation in Santa Cruz and Sucre Aprecia Blind Schools. experienced ophthalmologists and appropriate 7 Merin S, Lapithis AG, Horovitz D. et al: Childhood facilities for the treatment of congenital cataract. blindness in Cy prus. Am J Ophthalmol 1972, 74: 538-42. Conclusion 8 Baghdassarian SA, Tabbara KF. Childhood In countries with sophisticated medical care blindness in Lebanon. Am J Ophthamol 1975, 79: services, hereditary causes and factors operating 827-30. at the time of birth (e.g. hypoxia) are responsible 9 Tabbara KF, Badr IA. Changing patterns of for the majority of cases of childhood blindness. childhood blindness in Saudi Arabia. Br J 1985, 312-15. Better neonatal care of pre-term babies has Ophthamol 69: reduced neonatal mortality, but resulted in an 10 Foster A, Sommer A. Childhood Blindness and Corneal Ulceration in Africa. WHO 1986, 64: increase in morbidity including visual handicap. (5): 619-23. 23: 246-9. Genetic counselling and further improvements in \I Cullinan T. Epidemiology of Blindness in Clinical the management of pre-term infants could result Ophthalmology. Ed Miller, Sir S Wright Publ. in a reduction in childhood blindness in Europe 12 Cohen N, Rahman H, Sprague J, Jahl M, Leembuis and North America. E, Mitra M. Prevalence and determinants of In areas of the world with intermediate nutritional blindness in Bangladeshi children. medical services, intra-uterine infections, World Health Statistics Quarterly. 1985, 38: particularly rubella, remain an important 317-29. preventable cause of childhood blindness. \3 Chirambo MC et al. Blindness and visual 1986, Immunisation of infants with the combined impairment in southern Malawi. WHO Bull 64: 567-72. measles-rubella vaccine would reduce the 14 Sauter J1. Xerophthalmia and measles in Kenya. number of children born with the congenital Groningen: Van Denderen 1976. rubella syndrome. 15 Personal Observation Sebeta blind school 1986. In the large rural and urban slum areas of 16 Sauter, J1. Causes of Blindness in 19 schools for Asia, Africa and parts of South America, blind in Tanzania. Final report for Ministry of vitamin A deficiency, measles and the lack of eye Health, Dar-es-Salaam 1978. care services are responsible for 50-75 % of 17 Chirambo MC. 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